fMRI and Ghrelin in Obesity and Binge Eating Disorder

描述(申请人提供)：肥胖症在美国和全球的流行率持续上升。肥胖导致发病率和死亡率增加，尤其是糖尿病和心脏病。在寻求治疗的肥胖患者中，约有30%患有暴饮暴食障碍(Bed)。他们进食非常多的食物而不排便，就像神经性暴食症那样。床，最常见的特征饮食障碍，导致许多痛苦，并导致肥胖的发展。虽然心理因素已被研究，但对床的生物因素知之甚少。这项临床研究将集中在进餐后的大脑成像和肠道激素，以检查卧床和不卧床的受试者之间的差异。将有24个肥胖床(12米，12层)和24个体重匹配的肥胖非床(12米，12层)受试者。在一天中，摄取固定的液体餐(750毫升)，并抽血测量各种食欲激素，包括Ghrelin，PYY和GLP-1，在前后两小时内进行测量。预测结果是，与不卧床的受试者相比，空腹Ghrelin水平较低，餐后卧床降幅较小。与不卧床的受试者相比，床上的PYY和GLP-1的空腹水平较低，餐后PYY和GLP-1的增幅较小。另一天，只摄入水(750毫升)，以控制这些荷尔蒙的日变化。在固定食物或水后135分钟，将使用功能成像(FMRI)来检查大脑激活区对暴食、非暴食和非暴食的视觉和听觉刺激的反应。与床上其他刺激组相比，与非BED受试者相比，前额叶皮质等区域对暴饮暴食的反应更活跃。由于在没有饥饿的情况下经常会出现暴饮暴食，因此即使在美联储的状态下，更多的激活也预计会在床上的受试者中暴饮暴食。在第三天，将使用各种心理量表来评估饮食行为和情绪。将测量身体成分，以获得身体脂肪的百分比，以验证两组人的身体成分相似。这项关于大脑成像和与进餐相关的食欲激素的研究应该会提高我们对暴饮暴食障碍(Bed)潜在生物学因素的了解。这可能会导致诊断和治疗的改进，以帮助恢复正常的食欲、激素水平和在床上的大脑活动，这种疾病的患病率随着肥胖的增加而增加。

DESCRIPTION (provided by applicant): The prevalence of obesity continues to increase in the US and globally. Obesity results in increased morbidity and mortality, especially from diabetes and heart disease. Approximately 30% of obese individuals seeking treatment have binge eating disorder (BED). They ingest very large meals without purging afterwards as in bulimia nervosa. BED, the most common characterized eating disorder, causes much distress and contributes to the development of obesity. Although psychological factors have been studied, little is known about the biological factors of BED. This clinical research study will focus on brain imaging and gut hormones following a meal to examine differences between BED and non-BED subjects. There will be 24 obese BED (12 m, 12 f) and 24 weight-matched obese non-BED (12 m, 12 f) subjects. On one day, a fixed liquid meal (750 ml) will be ingested and blood drawn to measure various appetite hormones including ghrelin, PYY, and GLP-1, measured before and during a 2-hour period afterwards. The prediction is a lower fasting level of ghrelin and a smaller postprandial fall in BED compared to non-BED subjects. Also predicted are lower fasting levels and smaller postprandial increases of PYY and GLP-1 in BED compared to non-BED subjects. On another day, only water (750 ml) will be ingested as a control for diurnal variation in these hormones. At 135 min after the fixed meal or water, functional imaging (fMRI) will be employed to examine brain activation areas in response to visual and auditory stimuli of binge foods, nonbinge foods, and nonfoods. Greater activation is expected in such areas as the prefrontal cortex in response to binge foods relative to the other stimuli groups in BED than in nonBED subjects. Increased activation is also expected to binge food stimuli in the BED subjects even in the fed state as binge eating often occurs in the absence of hunger. On a third day, various psychological scales to assess eating behavior and mood will be administered. Body composition will be measured to obtain percentage body fat to verify similar body composition in the two groups. This study on brain imaging and meal-related appetite hormones should improve our knowledge of the underlying biological factors in Binge Eating Disorder (BED). This may lead to improved diagnosis and treatments to help restore normal appetite hormone levels and brain activity in BED, a disorder which is increasing in prevalence alongside obesity.